Light Intensity: The Role Player in Cucumber Response to Cold Stress

Low temperatures are a substantial limitation in the geographic distribution of warm-season crops such as cucumber (Cucumis sativus L.). Tolerance to low temperatures varies among different plant species and genotypes when changes in environmental cues occur. Therefore, biochemical and biophysical events should be coordinated to form a physiological response and cope with low temperatures. We examined how light intensity influences the effects of low temperature on photosynthesis and some biochemical traits. We used chlorophyll fluorescence imaging and polyphasic fluorescence transient to analyze cold stress damage by 4 °C. Photosynthetic Photon Flux Densities (PPFDs) of 0, 300, and 600 μmol m−2 s−1, in four accessions of cucumber, were investigated. The results show that the negative effects of cold stress are PPFD-dependent. The adverse effect of cold stress on the electron transport chain is more pronounced in plants exposed to 600 μmol m−2 s−1 than the control and dark-exposed plants, indicated by a disturbance in the electron transport chain and higher energy dissipation. Moreover, biochemical traits, including the H2O2 content, ascorbate peroxidase activity, electrolyte leakage, and water-soluble carbohydrate, increased under low temperature by increasing the PPFD. In contrast, chlorophyll and carotenoid contents decreased under low temperature through PPFD elevation. Low temperature induced a H2O2 accumulation via suppressing ascorbate peroxidase activity in a PPFD-dependent manner. In conclusion, high PPFDs exacerbate the adverse effects of low temperature on the cucumber seedlings.

Dopamine and Methamphetamine Differentially Affect Electron Transport Chain Complexes and Parkin in Rat Striatum: New Insight into Methamphetamine Neurotoxicity

Methamphetamine (METH) is a highly abused psychostimulant that is neurotoxic to dopaminergic (DAergic) nerve terminals in the striatum and increases the risk of developing Parkinson’s disease (PD). In vivo, METH-mediated DA release, followed by DA-mediated oxidative stress and mitochondrial dysfunction in pre- and postsynaptic neurons, mediates METH neurotoxicity. METH-triggered oxidative stress damages parkin, a neuroprotective protein involved in PD etiology via its involvement in the maintenance of mitochondria. It is not known whether METH itself contributes to mitochondrial dysfunction and whether parkin regulates complex I, an enzymatic complex downregulated in PD. To determine this, we separately assessed the effects of METH or DA alone on electron transport chain (ETC) complexes and the protein parkin in isolated striatal mitochondria. We show that METH decreases the levels of selected complex I, II, and III subunits (NDUFS3, SDHA, and UQCRC2, respectively), whereas DA decreases the levels only of the NDUFS3 subunit in our preparations. We also show that the selected subunits are not decreased in synaptosomal mitochondria under similar experimental conditions. Finally, we found that parkin overexpression does not influence the levels of the NDUFS3 subunit in rat striatum. The presented results indicate that METH itself is a factor promoting dysfunction of striatal mitochondria; therefore, it is a potential drug target against METH neurotoxicity. The observed decreases in ETC complex subunits suggest that DA and METH decrease activities of the ETC complexes via oxidative damage to their subunits and that synaptosomal mitochondria may be somewhat “resistant” to DA- and METH-induced disruption in mitochondrial ETC complexes than perikaryal mitochondria. The results also suggest that parkin does not regulate NDUFS3 turnover in rat striatum.

Age-Dependent Decline of NAD+ - Universal Truth or Confounded Consensus?

Nicotinamide adenine dinucleotide (NAD+) is an essential molecule involved in various metabolic reactions, acting as an electron donor in the electron transport chain and as a co-factor for NAD+-dependent enzymes. In the early 2000s, reports that NAD+ declines with aging introduced the notion that NAD+ metabolism is globally and progressively impaired with age. Since then, NAD+ became an attractive target for potential pharmacological therapies aiming to increase NAD+ levels to promote vitality and protect against age-related diseases. This review summarizes and discusses a collection of studies that report the levels of NAD+ with aging in different species (i.e., yeast, C. elegans, rat, mouse, monkey, and human), to determine whether the notion that overall NAD+ levels decrease with aging stands true. We find that, despite systematic claims of overall changes in NAD+ levels with aging, the evidence to support such claims is very limited and often restricted to a single tissue or cell type. This is particularly true in humans, where the development of NAD+ levels during aging is still poorly characterized. There is a need for much larger, preferably longitudinal, studies to assess how NAD+ levels develop with aging in various tissues. This will strengthen our conclusions on NAD metabolism during aging and should provide a foundation for better pharmacological targeting of relevant tissues.

A Model of Mitochondria in the Rat Hepatocyte

Mitochondria are a key player in several kinds of tissue injury, and are even the ultimate cause of certain diseases. In this work we introduce a new model of mitochondrial ATP generation in liver hepatocytes of the rat. Ischemia-reperfusion is an intriguing example of a non-equilibrium behaviour driven by a change in tissue oxygen tension. Ischemia involves prolonged hypoxia, followed by the sudden return of oxygen during reperfusion. During reperfusion, we predict that the build up of succinate causes the electron transport chain in the liver to temporarily be in a highly reduced state. This can lead to the production of reactive oxygen species. We accurately predict the timescale on which the electron transport chain is left in a reduced state, and we observe levels of reduction likely to lead to reactive oxygen species production. Aside from the above, we predict thresholds for ATP depletion from hypoxia, and we predict the consequences for oxygen consumption of uncoupling.

The atypical kinase ABC1K1 interacts with the EXECUTER pathway to promote chloroplast biogenesis.

Multiple chloroplast-to-nucleus signaling pathways contribute to the regulation of chloroplast biogenesis during plant greening. Here, we provide evidence for the direct implication of the atypical kinase ABC1K1. ABC1K1 is required for sufficient plastoquinone (PQ) allocation to the photosynthetic electron transport chain. Unexpectedly, mutation of abc1k1 suppresses greening and results in pale cotyledons under red light. This phenotype was not observed in other photosynthetic mutants and points to a specific signaling defect. Under red light, abc1k1 accumulated EXECUTER1 (EX1), a trigger of singlet oxygen (1O2) signaling. Consistent with the role of the FTSH metalloprotease in chloroplast biogenesis and EX1 degradation, the ftsh2 mutant var2, mimicked the greening defect of abc1k1 and accumulated EX1 under red light. We propose that this novel ABC1K1-dependent signal is required for chloroplast biogenesis to progress in challenging light conditions.